The blood supply to that portion of the stomach is from a large submucosal artery arising directly from the left gastric artery. Osoephagogastroscopy (OGD) can successfully identify the lesions in approximately 82% of patients. Approximately 49% of the lesions are identified during the initial endoscopic examination, while 33% require more than one OGD for confident identification

[17–19]. The remainder of the patients with Dieulafoy’s lesions is identified intraoperatively or angiographically [20, 21]. Endoscopic ultrasound can be a useful tool in confirming the diagnosis of a Dieulafoy’s lesion, by showing a tortuous submucosal vessel adjacent to the mucosal defect. Angiography, during Smoothened Agonist concentration active bleeding has been helpful in a small number of cases in which initial endoscopy failed to show the bleeding source. It has been tentatively suggested that, in selected cases where Selleck MS275 experienced radiological, endoscopic and surgical staff are available, thrombolytic therapy to precipitate bleeding can be used electively

as an adjunct to diagnostic angiography to help in localizing Dieulafoy’s lesion [22]. Other reported diagnostic methods include CT and enteroclysis learn more [23]. For acute and massive gastrointestinal haemorrhage, immediate embolisation can stop bleeding and maintain vital signs of positive bleeders [24]. Endoscopic techniques used in the treatment include epinephrine injection followed by bipolar electrocoagulation, monopolar electrocoagulation,

injection sclerotherapy, heater probe, laser photocoagulation, Casein kinase 1 haemoclipping or banding [2]. Rarely, surgical removal of the lesion may be needed and is recommended only if other treatment options have not been successful. Endoscopic therapy is said to be successful in achieving permanent haemostasis in 85% of cases. Of the remaining 15% in whom re-bleeding occurs, 10% can successfully be treated by repeat endoscopic therapy and 5% may ultimately require surgical intervention [19, 25]. The endoscopic criteria proposed to define DL are: 1) Active arterial spurting or micropulsatile streaming from a minute mucosal defect or through normal surrounding mucosa, 2) Visualization of a protruding vessel with or without active bleeding within a minute mucosal defect or through normal surrounding mucosa, and 3) Fresh, densely adherent clot with a narrow point of attachment to a minute mucosal defect or to normal appearing mucosa [24, 26]. DL is characterized by a single large tortuous arteriole in the submucosa which does not undergo normal branching, or one of the branches retain high caliber of about 1–5 mm which is more than 10 times the normal diameter of mucosal capillaries.